Evidence map›Paper›PMID 21415385›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2011

C-reactive protein polarizes human macrophages to an M1 phenotype and inhibits transformation to the M2 phenotype.

Sridevi Devaraj, Ishwarlal Jialal

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
5.3field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

81 citing papers in PubMed, 157 citations in OpenAlex.

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21 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 2 countries.

Sridevi DevarajLaboratory for Atherosclerosis and Metabolic Research, University of California, Davis, Medical Center, Sacramento, CA 95817, USA.
Ishwarlal Jialal
Veterans Health Administration · US

Funding

CRP, Diabetes, AtherothrombosisR01HL074360 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI JIALAL, ISHWARLAL · 2004 to 2010
$2.3M
CLINICAL STUDIES IN NUTRITION AND METABOLISMK24AT000596 · NCCIH · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI JIALAL, ISHWARLAL · 2000 to 2009
$1.3M
NCCIH NIH HHS K24 AT000596NCCIH NIH HHS K24AT00596NHLBI NIH HHS R01 HL074360NHLBI NIH HHS R01HL74360
6 · The paper itself

Abstract

objectiveInflammation is pivotal in atherosclerosis. Monocyte-macrophages are crucial in atherosclerosis. Monocytes can develop into subsets: classically (M1) or alternatively (M2) activated cells. Several studies point to a proinflammatory role for C-reactive protein (CRP). Because there is a paucity of data on the effects of CRP on macrophage phenotype, we tested effects of CRP on macrophage polarization. METHODS AND

resultsMonocytes were incubated with CRP (0 to 50 μg/mL) and differentiated into macrophages for 7 days. Phenotypic characterization of M1 and M2 macrophages was performed using flow cytometry. CRP treatment resulted in increased population of M1 macrophages (tumor necrosis factor [TNF]/interleukin [IL]-12/C-C chemokine receptor 2, TNF/IL-12/monocyte chemotactic protein-1, or TNF/IL-1/IL-12). These effects were not abrogated by polymixin B or small interfering RNA to Toll-like receptor-4, but they were abrogated by boiled CRP. Administration of human CRP to rats in vivo increased polarization of macrophages to M1 phenotype compared with human serum albumin. When macrophages were primed to the M2 phenotype with IL-4, addition of CRP resulted in significantly increased secretion of TNF-α, MCP-1, and IL-1 and conversion of macrophages from the M2 to the M1 phenotype. CRP failed to prime macrophages to the M1 phenotype in presence of CD32/CD64 small interfering RNA or dominant-negative nuclear factor kappa B.

conclusionCollectively, these results further support a role for CRP in promoting differentiation of human monocytes toward a proinflammatory M1 phenotype.

Indexed as

AnimalsCell DifferentiationCell PolarityCells, CulturedC-Reactive ProteinHumansInflammationInterleukin-4MacrophagesMonocytesNF-kappa BPhenotypePolymyxin BRatsReceptors, IgGSerum AlbuminC-Reactive ProteinInterleukin-4NF-kappa BPolymyxin BReceptors, IgGSerum Albumin

Identifiers

PMID21415385
PMCPMC3099471
OpenAlexW2150401131

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.